The article “Demystifying NSAIDs” (Clinical Update, March) was a concise and interesting summary of the many uses of these drugs in ocular disease. Two points, however, caught my attention.

First, although some relatively exotic and unproven uses of these drugs (such as in dry eye and blepharitis) are mentioned, other well-established uses of these drugs where they have been used effectively, such as episcleritis and scleritis, in which they are of use both topically and systemically, are ignored.

Second and more serious, the article states “NSAIDs appear to mitigate the increase in IOP caused by corticosteroids.” Although there are articles showing that the use of steroids can be decreased by using NSAIDs in several clinical scenarios, notably after cataract surgery, the statement that these drugs can actually mitigate the IOP rise caused by steroid drops in steroid responders is a dangerous one.

I am aware of only one article that even suggests such an effect,¹ and the author of that article used an experimental formulation of NSAID not currently available on the market.

The generalized statement that NSAIDs “appear to mitigate the increase in IOP caused by steroids” must be tempered with the caution that this practice is not standard of care, is unproven and, indeed, any patient on prolonged topical NSAIDs therapy needs IOP monitoring.

In “Endophthalmitis: Cataract Controversy” (June 2004), some comments regarding the “Topical Prophylaxis With Moxifloxacin Prevents Endophthalmitis in a Rabbit Model” study¹ were incorrect.

The article states that all the rabbits in the placebo group were infected and none in the Vigamox group. This is untrue.

According to Regis P. Kowalski, MD’s, American Journal of Ophthalmology paper, only 50 percent of the placebo rabbits actually developed an infection. Upon closer reading of the AJO article, I questioned aspects of this paper. (The choice of inoculum and the Staphylococcus aureus strain with an MIC of 0.19 micrograms per milliliter raised red flags for me.)

In a different study, the same investigators from the Campbell Lab in Pittsburgh studied two resistant S. aureus strains whose MIC values were 12 and 64 µg/mL, and found that Zymar (gatifloxacin) was able to cure each keratitis infection. In that study, they quantified the number of viable bacteria recovered. While the Zymar study reported change in bacterial counts before and after treatment, the Vigamox study only reported culture positivity.

To address another matter, the article states the newer antibiotics are able to penetrate into the anterior chamber because that is where the bacteria are in the eye. Keeping in mind that the most common route of infection is through introduction via the normal flora on the ocular surface and surrounding structures, this is why it is important to use a fast-acting antimicrobial solution that rapidly kills bacteria on the ocular surface.

It is essential that physicians critique animal studies. In this case, the clinical correlation with human surgical prophylaxis might be more beneficial with more virulent bacteria. Further studies should be conducted in this area.

In “Acquired Ptosis: Evaluation and Management” (Ophthalmic Pearls, February) on page 32 under “Anatomic Considerations,” the article incorrectly states “the eyelashes insert into the inferior border of the tarsal plate to extend out through the gray line.” The eyelashes do not insert into the tarsus. And the lash line is distinctly anterior to the gray line (which represents the muscle of Riolan). EyeNet regrets the error.

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